The role of endogenous reactive oxygen species in oxymatrine-induced caspase-3-dependent apoptosis in human melanoma A375 cells

2010 ◽  
Vol 21 (5) ◽  
pp. 494-501 ◽  
Author(s):  
Yingfan Zhang ◽  
Huanhai Liu ◽  
Jiyang Jin ◽  
Xiaohai Zhu ◽  
Lixuan Lu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Caspase 3 ◽  
Reactive Oxygen ◽  
Human Melanoma ◽  
Oxygen Species ◽  
Endogenous Reactive Oxygen Species ◽  
A375 Cells

Ascorbic acid improves mitochondrial function in liver of arsenic-treated rat

2010 ◽  
Vol 26 (5) ◽  
pp. 265-272 ◽  
Author(s):  
Sohini Singh ◽  
Suresh Vir Singh Rana
Keyword(s):  
Reactive Oxygen Species ◽  
Ascorbic Acid ◽  
Mitochondrial Function ◽  
Caspase 3 ◽  
Succinic Dehydrogenase ◽  
Reactive Oxygen ◽  
Ultrastructural Changes ◽  
Arsenic Toxicity ◽  
Oxygen Species

Arsenic is an ubiquitous and well-documented carcinogenic metalloid. The most common source of arsenic is drinking water. The mechanism of arsenic toxicity in a cell has historically been centered around its inhibitory effects on cellular respiration and mitochondrial injury. Ascorbic acid, a low molecular weight, water-soluble antioxidant, improves the reduced glutathione (GSH) status by recycling oxidized glutathione. Ascorbic acid can improve mitochondrial function by improving the thiol status; thereby preventing reactive oxygen species— mediated damage to liver as well as kidney. Ascorbic acid has been shown to protect membrane and other cellular compartments by regenerating vitamin E. Therefore, ascorbic acid seems to be a suitable protective factor against arsenic toxicity. Present reports describe the effect of ascorbic acid on oxidative phosphorylation, adenosine triphosphatase (ATPase), succinic dehydrogenase, caspase-3 and apoptosis in the liver of rats treated with arsenic trioxide (AsIII). Ultrastructural changes in the mitochondria have also been reported. We show that cotreatments with ascorbic acid and AsIII improve mitochondrial structure and function. We attribute these improvements mainly to antioxidative role of ascorbic acid. Apoptosis was restricted due to caspase-3 inhibition. Ascorbic acid could protect DNA from the attack of reactive oxygen species generated by AsIII. Consequently its events led to improved ADP:O ratio, normalized ATPase activity and restored the activity of succinic dehydrogenase. Overall, results support the protective role of ascorbic acid against As III-induced liver injury.

Quinalizarin induces cycle arrest and apoptosis via reactive oxygen species‐mediated signaling pathways in human melanoma A375 cells

2019 ◽  
Vol 80 (8) ◽  
pp. 1040-1050 ◽  
Author(s):  
Ying‐Hua Luo ◽  
Jin‐Qian Li ◽  
Yi Zhang ◽  
Jia‐Ru Wang ◽  
Wan‐Ting Xu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Signaling Pathways ◽  
Reactive Oxygen ◽  
Human Melanoma ◽  
Oxygen Species ◽  
Cycle Arrest ◽  
A375 Cells
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